Coronary artery disease (CAD) is now an important cause of premature
death in people with HIV but the causes of accelerated CAD are poorly
understood. Epicardial adipose tissue (EAT) is metabolically-active and
thought to contribute to CAD development. We tested the hypothesis that
abnormal coronary endothelial function (CEF), an early marker and mediator
of atherosclerosis, is related to the amount of local pericoronary EAT in
HIV. We studied 36 participants with HIV and no CAD (HIV+CAD−), 15
participants with HIV and known CAD (HIV+CAD+), and 14 age-matched, healthy
participants without HIV (HIV−CAD−). To measure CEF, coronary
MRI was performed before and during isometric handgrip exercise (IHE), an
endothelial-dependent stressor. EAT was measured with MRI at the same
imaging plane as CEF. CEF was significantly depressed, as measured by IHE-induced
%
coronary cross sectional area (CSA) change, in HIV+CAD− and HIV+CAD+
as compared to HIV−CAD−participants
( p< 0.0001). EAT thickness was significantly
greater in HIV+CAD− and HIV+CAD+ participants as compared to
HIV−CAD− participants ( p= 0.001). There was a
significant inverse relationship between CEF and local EAT thickness and
area (R=−0.48 and R=−0.51 respectively,
p< 0.0001 for both) among participants with HIV
even after adjustment for cardiovascular risk factors. In participants with
multiple CEF measures, CEF was lower in segments with higher EAT, other
factors being equivalent. There is a significant relationship between increased
metabolically-active EAT and depressed local CEF in people with HIV,
consistent with the hypothesis that increased epicardial fat contributes to
accelerated CAD in persons with HIV.